Prevention of Mercury-Induced Cardiotoxicity After Short-Term Egg White Hydrolysate Supplementation in Rats
摘要
Mercury exposure triggers localized oxidative stress, playing a central role in its detrimental effects, because toxic levels of ROS induce lipid peroxidation, promote protein oxidation and nitration, and nucleic acid oxidation and damage. Egg white hydrolysate (EWH), a functional food, is a protein extract that has promising capabilities against metal-induced cardiovascular damage. However, its potential in preventing the acute effects of mercury exposure remains unexplored. This study evaluated the preventive efficacy of 3 days, a short-term EWH treatment against the subsequent acute exposure to HgCl2 in isolated left ventricle papillary muscles. Male Wistar rats were divided into four groups: Control, EWH, HgCl2 and EWH + HgCl2. Animals received filtered water or EWH (1 g/kg/day) via oral gavage for 3 days as pre-treatment. Subsequently, papillary muscles were isolated, and then HgCl2 and EWH + HgCl2 groups were exposed to 6 nM HgCl2 for 60 min. Results revealed that acute HgCl2 exposure impaired force generation, positive and negative time derivatives of force, indicating contractile dysfunction. Notably, these effects were absent in the EWH + HgCl2 group. Furthermore, HgCl2 exposure depressed post-rest potentiation, inotropic response protocols to calcium and isoproterenol while the EWH + HgCl2 group exhibited comparable responses to the control group. Besides that, the increase in ROS levels induced by HgCl2 in vitro was prevented by EWH pre-treatment. In conclusion, EWH demonstrated a cardioprotective effect by preserving contractile function, maintaining physiological inotropic responses, and preventing ROS accumulation with a remarkably brief 3-day pre-treatment period, highlighting its potential against the deleterious effects of acute mercury exposure, particularly in unavoidable or unpredictable exposures.
Graphical Abstract